Increased expression of fatty acid binding protein 4 in lungs of preterm rats afterhyperoxic lung injury

WANG Wei, CUI Zhi-Rui, CAI Li-Xia, LUO Xiao-Ping

Chinese Journal of Contemporary Pediatrics ›› 2014, Vol. 16 ›› Issue (11) : 1149-1153.

PDF(2086 KB)
PDF(2086 KB)
Chinese Journal of Contemporary Pediatrics ›› 2014, Vol. 16 ›› Issue (11) : 1149-1153. DOI: 10.7499/j.issn.1008-8830.2014.11.016
EXPERIMENTAL RESEARCH

Increased expression of fatty acid binding protein 4 in lungs of preterm rats afterhyperoxic lung injury

  • WANG Wei1, CUI Zhi-Rui1, CAI Li-Xia1, LUO Xiao-Ping2
Author information +
History +

Abstract

Objective To study the expression of fatty acid binding protein 4 (FABP4) in lungs and bron choalveolar lavage fluid (BALF) of preterm rats exposed to 60% O2 and to elucidate the relationship between thechanges of FABP4 expression and the pathogenesis of bronchopulmonary dysplasia (BPD). Methods Hyperoxiclung injury was induced by exposing to 60% O2 in Spraque-Dawley rats within 6 hours after birth. Rats exposedto air were used as the control group. The lungs from groups aged postnatal days 3, 7 and 14 were removed and dissected from the main bronchi for analysis. Eight rats of each group were used to assess expression of FABP4 inlungs by immunohistochemistry and ELISA. Lung FABP4 mRNA levels were measured by semi-quantitative reversetranscription polymerase chain reaction. The levels of FABP4 in BALF were measured using ELISA. Results FABP4 immunoreactivity was detected in the majority of alveolar macrophages, bronchial epithelial cells and endothelial cells.FABP4 protein levels in lung tissues in the hyperoxic exposure group increased significantly compared with the controlgroup on days 3, 7 and 14 after birth (P<0.05), and FABP4 mRNA levels in lung tissues also increased significantly inthe hyperoxic exposure group compared with the control group on days 7 and 14 after birth (P<0.05). The hyperoxicexposure group demonstrated increased FABP4 levels in BALF compared with the control group on days 7 and 14after birth (P<0.05). Conclusions FABP4 levels increase in preterm rat lungs after hyperoxic lung injury, which maycontribute to the pathogenesis of BPD.

Key words

Hyperoxia / Fatty acid binding protein 4 / Bronchopulmonary dysplasia / Rats

Cite this article

Download Citations
WANG Wei, CUI Zhi-Rui, CAI Li-Xia, LUO Xiao-Ping. Increased expression of fatty acid binding protein 4 in lungs of preterm rats afterhyperoxic lung injury[J]. Chinese Journal of Contemporary Pediatrics. 2014, 16(11): 1149-1153 https://doi.org/10.7499/j.issn.1008-8830.2014.11.016

References

[1] Hadchouel A, Delacourt C. Premature infants bronchopulmonary dysplasia:past and present[J]. Rev Pneumol Clin, 2013, 69(4):207-216.
[2] Madurga A, Mizíková I, Ruiz-Camp J, et al. Recent advances in late lung development and the pathogenesis of bronchopulmonary dysplasia[J]. Am J Physiol Lung Cell Mol Physiol, 2013, 305(12):893-905.
[3] Talwar T, Srivastava MV. Role of vascular endothelial growth factor and other growth factors in post-stroke recovery[J]. Ann Indian Acad Neurol, 2014, 17(1):1-6.
[4] 王伟, 韦伟, 王安茹, 等. 60%氧暴露对早产大鼠肺血管内 皮生长因子及其受体表达的影响[J]. 中华围产杂志, 2007, 9(3):153-159.
[5] 韦伟, 王伟, 宁琴, 等. 早产鼠高氧暴露后肺组织血管内皮 生长因子和一氧化氮合酶的动态变化及相互关系[J]. 中国当 代儿科杂志, 2007, 9(5):473-478.
[6] Ghelfi E, Yu CW, Elmasri H, et al. Fatty acid binding protein 4 regulates VEGF-induced airway angiogenesis and inflammation in a transgenic mouse model:implications for asthma[J]. Am J Pathol, 2013, 182(4):1425-1433.
[7] Ozdemir OM, Gözkeser E, Bir F, et al. The effects of resveratrol on hyperoxia-induced lung injury in neonatal rats[J]. Pediatr Neonatol, 2014, 124(10):1875-1891.
[8] Levesque BM, Kalish LA, Winston AB, et al. Low urine vascular endothelial growth factor levels are associated with mechanical ventilation, bronchopulmonary dysplasia and retinopathy of prematurity[J]. Neonatology, 2013, 104(1):56-64.
[9] Esquibies AE, Karihaloo A, Quaggin SE, et al. Heparin binding VEGF isoforms attenuate hyperoxic embryonic lung growth retardation via FLK1-neuropilin-1-PKC dependent pathway[J]. Respir Res, 2014, 15:32.
[10] Ghelfi E, Karaaslan C, Berkelhamer S, et al. Fatty acid-binding proteins and peribronchial angiogenesis in bronchopulmonary dysplasia[J]. Am J Respir Cell Mol Biol, 2011, 45(3):550-556.
[11] Elmasri H, Karaaslan C, Teper Y, et al. Fatty acid binding protein 4 is a target of VEGF and a regulator of cell proliferation in endothelial cells[J]. FASEB J, 2009, 23(11):3865-3873.
[12] Hoo RL, Lee IP, Zhou M, et al. Pharmacological inhibition of adipocyte fatty acid binding protein alleviates both acute liver injury and non-alcoholic steatohepatitis in mice[J]. J Hepatol, 2013, 58(2):358-364.
[13] Shum BO, Mackay CR, Gorgun CZ, et al. The adipocyte fatty acid-binding protein aP2 is required in allergic airway inflammation[J]. J Clin Invest, 2006, 116(8):2183-2192.
[14] Hadchouel A, Franco-Montoya ML, Delacourt C. Altered lung development in bronchopulmonary dysplasia[J]. Birth Defects Res A Clin Mol Teratol, 2014, 100(3):15-17.
[15] Sun H, Choo-Wing R, Fan J, et al. Small molecular modulation of macrophage migration inhibitory factor in the hyperoxiainduced mouse model of bronchopulmonary dysplasia[J]. Respir Res, 2013, 1465(28):14-27.
PDF(2086 KB)

Accesses

Citation

Detail

Sections
Recommended

/